Synthese yon SH-Phthalazino[ 1.2-b]chinazolonen-(S)Aus dem Institut fur Organische Chemie der Universitat Greifswald
In dem von J. THIELE und E. DRALLE~) aus Acetonylaceton und Aminoguanidin in mineralsaurer Losungerhaltenen Kondensationsprodukt liegt das 1 -Guanidino-2.5-dimethyl-pyrrol vor. Thiosemicarbazid reagiert unter gleichen Bedingungen rnit 2 Moll. Aceton ylaceton zum C.N-Bis-[2.5-dimethyl-pyrryl-( I)]-thioformamid.Dagegen entsteht bei derselben Umsetzung in essigsaurer Losung das Bis-thiosemicarbazon des Acetonylacetons, das bei der Einwirkung von wasserfreier Ameisensaure in 1-Thioureido-2.5-dimethyl-pyrrol ubergeht. -Aus I .2-Dibenzoyl-athan und Thiosemicarbazid erhalt man das 1 -Thioureido-2.5-diphenyl-pyrrol. -1.2-Diacetyl-athylen setzt sich mit den Hydrazinderivaten der Kohlensaure zu den entsprechenden Bis-hydrazonen um. Beim 1.2-Dibenzoylathylen sind letztere nur selten isolierbar, da sich meist das 3.6-Diphenylpyridazin bildet. -Von einigen Verbindungen wurden die UV-bzw. 1R-
The influence of dietary fat on the fatty acid composition of liver and adipose tissue lipids was investigated after 4 and 19 weeks of high-fat feeding (50% fat) in comparison to low-fat feeding (3% fat), beginning in the sixth week of age. In rats fed the low-fat diet or an usual pellet diet the fatty pattern of liver triglycerides (TG) was equal to that of adipose tissue, while there were no similarities to the diet. In total liver lipids a constant fatty acid profile was observed, independently of the duration of feeding. High fat feeding results several changes in the fatty acid pattern of liver lipids. While after 4 weeks the fatty acids of liver TG more closely resembled the dietary fatty acids than those of adipose tissue, after 19 weeks of feeding the fatty acid composition of liver TG is comparable with that of adipose tissue. Not all rats fed the high fat diet rendered obese. It could be shown that in rats with higher lipid concentrations in the liver only the fatty acid pattern of liver phospholipids has been altered, while the composition of TG, which are the lipids primarily increased, was not changed.
Diet-induced obesity in rats can be produced by high-fat feeding. Comparing high-fat with low-fat feeding, the present study was designed to characterize the phases of development of obesity. In the dynamic phase, male rats were investigated at the age of 9-10 weeks after feeding the diets for 4-5 weeks. In the static phase, the animals at the age of 24-26 weeks were tested after 20-22 weeks of the nutritional regime. In this phase, the effects of switching high-fat to low-fat diet for 4 weeks were also examined. Fractionating lipid extracts by thin layer chromatography the concentrations of several lipids in epididymal adipose tissue, in serum, and in liver were determined. In liver, the enhancement of cholesteryl-ester (CE) concentration after high-fat feeding besides the accumulation of triglycerides (TG) is remarkable. Cell fractionation studies of the livers by differential ultracentrifugation showed the major part of the accumulated CE in the supernatant. In vitro incorporation of (1-14C)acetate and (2-14C)mevalonate into liver slices indicated that cholesterol synthesis in the liver of the obese rats was not increased. Although the offered fat diet with 0.1% of cholesterol can not be considered as high in cholesterol, the 2.5-fold higher amount of the high-fat diet in comparison with the low-fat diet (0.04% cholesterol) could be responsible for the enlargement of CE in the liver of the fat fed rats. This possibility was proved by measurement of the cholesterol absorption and transport to the liver after oral administration of (4-14C)cholesterol. Estimation of TG secretion rates of the liver using Triton WR 1339 pointed out higher rates in the obese rats in the dynamic phase. In the static phase, the rates were not different between both feeding groups, while fat restriction in the food produced a striking increase of TG secretion. It is assumed that only in the dynamic phase metabolism is able to compensate the liver TG accumulation by an enhanced transport to the adipose tissue. In the static phase this ability is diminished but not lost.
The influence of thyroxine, estradiol and testosterone on the triacylglycerol (TG) secretion rate out of the liver into the blood as well as on concentrations of FFA, triglycerides, and glucose in serum was determined. All of these experiments were carried out under different nutritional conditions (non-fasting, and 10 or 16 h fasting, respectively). Accordingly the results after hormone application were compared with three groups of controls. Within these control groups increasing time of fasting caused exclusively an enhancement of FFA concentrations, while the TG secretion rate and other parameters were not influenced. Concerning all hormones effects on several lipid parameters have been observed. In particular, a decrease of FFA concentrations in comparison with controls after 16 h fasting was evident. In these cases, the TG secretion rate and TG concentration in serum were simultaneously lowered. Both alterations may be a consequence of a diminished mobilization of FFA in adipose tissue. Increases of FFA concentrations in serum after hormone application, compared with the corresponding controls, only occurred after administration of thyroxine and testosterone, while changes of the TG secretion rate and the TG concentration in serum were scarcely observed. Final remarks about the actual influence of hormones on the investigated parameters, especially TG secretion rate were drawn including results of a previous paper, where catecholamines, insulin, and prednisolone had been tested under the same conditions.
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